First emerging objective experimental evidence of hearing impairment following subarachnoid haemorrhage; Felix culpa, phonophobia, and elucidation of the role of trigeminal ganglion.

The exact mechanism of phonophobia induced by subarachnoid hemorrhage (SAH) has not been understood well. This subject was investigated. This study was conducted on 25 rabbits. They divided into three groups: Five as control, five as SHAM, 20 as SAH group. All animals objected to 85 dB impulse noise by daily periods, and their phonophobic score values were examined by daily periods for 20 days. Their brains, trigeminal ganglia were extracted bilaterally. The normal and degenerated neuron densities of trigeminal ganglia were examined by stereological methods and compared with phonophobia scores. Phonophobic score was 19-17, mean live neuron density (LND) of the trigeminal ganglia was 16.321 ± 2.430/mm, and degenerated neuron density (DND) was 1.15 ± 0.120/mm in animals of control groups ( = 5). The phonophobic score was 17-14, LND: 14.345 ± 1.913/mm, DND of the trigeminal ganglia was 1.150 ± 0.110/mm in SHAM group ( = 5). The phonophobic score was 14-8, LND: 12.987 ± 1.966/mm, mean DND of the trigeminal ganglia was 2.520 ± 510/mm in animals with high phonophobia scores ( = 6). The phonophobic score was 7-4, LND: 9.122 ± 1.006, mean DND of the trigeminal ganglia was 5.820 ± 1.610/mm, in animals with fever phonophobia scores ( = 9). An inverse relationship between DND trigeminal ganglion (TGG) and phonopobic score was found. The paralysis of tensor tympani muscle owing to trigeminal ganglia ischemia may be responsible for phonophobic clinical state in animals with SAH. In addition, there seems to be an important concern for the verbal component of GCS in SAH. These two important findings have not been published previously.